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Differential diagnosis of a vanishing brain space occupying
lesion in a child
Sherifa A Hamed, Mohamad A Mekkawy, Hosam Abozaid
Sherifa A Hamed, Department of Neurology and Psychiatry,
Assiut University Hospital, Assiut 71516, Egypt
Mohamad A Mekkawy, Department of Oncology, Assiut
University Hospital, Assiut 71516, Egypt
Hosam Abozaid, Department of Radiology, Assiut University
Hospital, Assiut 71516, Egypt
Author contributions: All the authors equally contributed to
this work.
Institutional review board statement: This study was
reviewed by and received exemption from the Assiut UniversityHospital Institutional Review Board.
Informed consent statement: The study participant provided
written informed consent for inclusion in this case report.
Conflict-of-interest statement: The authors declared no
potential conflicts of interest with respect to the research,
authorship, and/or publication of this article.
Open-Access: This article is an open-access article which was
selected by an in-house editor and fully peer-reviewed by external
reviewers. It is distributed in accordance with the Creative
Commons Attribution Non Commercial (CC BY-NC 4.0) license,
which permits others to distribute, remix, adapt, build upon thiswork non-commercially, and license their derivative works on
different terms, provided the original work is properly cited and
the use is non-commercial. See: http://creativecommons.org/
licenses/by-nc/4.0/
Correspondence to: Dr. Sherifa A Hamed, MD, ConsultantNeurologist, Professor, Department of Neurology and
Psychiatry, Assiut University Hospital, Floor # 7, Room # 4,
Assiut 71516, Egypt. [email protected]
Telephone: +2-88-2371820
Fax: +2-88-2333327
Received: April 15, 2015
Peer-review started: April 18, 2015First decision: May 13, 2015
Revised: June 30, 2015
Accepted: August 4, 2015
Article in press: August 7, 2015
Published online: November 16, 2015
Abstract
We describe clinical, diagnostic features and follow up
of a patient with a vanishing brain lesion. A 14-year-
old child admitted to the department of Neurology at
September 2009 with a history of subacute onset of
fever, anorexia, vomiting, blurring of vision and right
hemiparesis since one month. Magnetic resonanceimaging (MRI) of the brain revealed presence of intra-
axial large mass (25 mm × 19 mm) in the left temporal
lobe and the brainstem which showed hypointense
signal in T1W and hyperintense signals in T2W and
fluid attenuated inversion recovery (FLAIR) images
and homogenously enhanced with gadolinium (Gd). It
was surrounded by vasogenic edema with mass effect.
Intravenous antibiotics, mannitol (2 g/12 h per 2 d)
and dexamethasone (8 mg/12 h) were given to relief
manifestations of increased intracranial pressure. Whole
craniospinal radiotherapy (brain = 4000 CGy/20 settings
per 4 wk; Spinal = 2600/13 settings per 3 wk) was
given based on the high suspicion of neoplastic lesion(lymphoma or glioma). Marked clinical improvement (up
to complete recovery) occurred within 15 d. Tapering
of the steroid dose was done over the next 4 mo.
Follow up with MRI after 3 mo showed small lesion in
the left antero-medial temporal region with hypointense
signal in T1W and hyperintense signals in T2W and
FLAIR images but did not enhance with Gd. At August
2012, the patient developed recurrent generalized
epilepsy. His electroencephalography showed the
presence of left temporal focus of epileptic activity.
MRI showed the same lesion as described in the follow
up. The diffusion weighted images were normal. Theseizures frequency was decreased with carbamazepine
therapy (300 mg/12 h). At October 2014, single
voxel proton (1H) MR spectroscopy (MRS) showed
CASE REPORT
956 November 16, 2015|Volume 3|Issue 11|WJCC|www.wjgnet.com
Submit a Manuscript: http://www.wjgnet.com/esps/Help Desk: http://www.wjgnet.com/esps/helpdesk.aspx
DOI: 10.12998/wjcc.v3.i11.956
World J Clin Cases 2015 November 16; 3(11): 956-964 ISSN 2307-8960 (online)
© 2015 Baishideng Publishing Group Inc. All rights reserved.
World Journal of
Clinical CasesW J C C
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reduced N-acetyl-aspartate (NAA)/creatine (Cr), choline
(Cho)/Cr, NAA/Cho ratios consistent with absence ofa neoplasm and highly suggested presence of gliosis. A solitary brain mass in a child poses a considerablediagnostic difficulty. MRS provided valuable diagnosticdifferentiation between tumor and pseudotumor lesions.
Key words: Vanishing brain mass; Gliosis; Unconfirmeddiagnosis; Lymphoma; Granuloma
© The Author(s) 2015. Published by Baishideng Publishing
Group Inc. All rights reserved.
Core tip: A vanishing brain space occupying lesionis defined as reduction or disappearance of a brainlesion spontaneously or after steroid treatment to≤ 70% of its size before establishing its definitivediagnosis. A vanishing solitary neoplastic/non-neoplastic(pseudotumor) (e.g. , infection/abscess, granuloma,radiation necrosis, multiple sclerosis) brain massin a child poses a considerable diagnostic difficultyparticularly deeply seated lesions in which tissuediagnosis is difficult to be done. In clinical practice,neuroimaging has to be done every 6-12 mo for at least
3-5 years to follow up after complete remission of thepatient. Magnetic resonance spectroscopy (MRS) hasbeen proved to be valuable for diagnostic differentiationbetween tumor and pseudotumor lesions. MRS providesinformation related to the metabolic activity in the culpritlesion (e.g. , neoplastic processes, demyelination, cellnecrosis or gliotic changes).
Hamed SA, Mekkawy MA, Abozaid H. Differential diagnosis of
a vanishing brain space occupying lesion in a child. World J Clin
Cases 2015; 3(11): 956-964 Available from: URL: http://www.
wjgnet.com/2307-8960/full/v3/i11/956.htm DOI: http://dx.doi.
org/10.12998/wjcc.v3.i11.956
INTRODUCTION
Cases with solitary brain space occupying lesions
(e.g., tumor, intracranial infection/abscess, granuloma,
neurocystocercosis, tuberculoma, multiple sclerosis)
may pose a diagnostic difculty particularly when brain
biopsy can’t be done due to deep location of the lesion.
For such cases, clinicians often start corticosteroids
to reduce manifestations of increased intracranial
pressure (ICP) (caused by the intracranial mass and
the surrounding vasogenic edema) and to give brain
radiation if there is a high suspension for the presence
of malignant lesion[1,2]
. Also such patients should be
routinely followed by magnetic resonance imaging (MRI)
even after the disappearance of the enhancing lesion for
at least 3-5 years[3]
. The disappearance or decrease of
the initial brain space occupying lesion (SOL) volume to≤ 70% either spontaneously or after steroid treatment
before establishing the definitive diagnosis, has been
referred as a vanishing brain lesion[4]
.
In the last decade, magnetic resonance spectro-
scopy (MRS) has been considered as a diagnostic test
which helped to distinguish normal from abnormal
brain tissue. Proton (1H) MRS measures some
unique tissue metabolites which provide valuable
information regarding the severity of the brain lesion,pathogenesis, prognosis and response to therapy.
Briefly, in MRS, peaks which are proportional to the
concentration of the given metabolite, are arranged
along a at baseline according to their radiofrequency
(measured in units called parts per million or ppm)[5]
.
The most commonly dened brain metabolites (1H-MRS
spectrum) in which their patterns can be observed and
correlate with different types of lesions (from right to
left) include: free lipids (Lip), lactate (Lac), N-acetyl-
aspartate (NAA), glutamate/glutamine (Glx), creatine
(Cr)/phosphocreatine (the Cr peak), choline (Cho; the
Cho peak), and myo-inositol (mI). In spectra obtained
at long echo time (≤ 135 ms), the peaks for NAA, Cr,Cho, and lactic acid are prominent and sharp. They
are also detected and quantied at short echo time (≥
30 ms) MRS. In contrast, Lip, Glx and mI signals are
detected only in short echo time MRS. In normal brain,
NAA is synthesized in neurons, diffuses along axons
and broken down in oligodendrocytes. In MRS, NAA is a
marker of intact number of neurons in gray matter and
the density of intact axons in white matter. The most
prominent peak of NAA in MRS is the resonance at 2.0
ppm and it has concentration of 7.9-16.6 mmol/kg.
NAA is a non-specic marker as its value is reduced in
any disease associated with neuronal or axonal loss[6]
.Cr is present at higher concentrations in the glia and
it is a marker of brain energy. The most prominent
peak of Cr in MRS is the resonance at 3.0 ppm and
concentration of 5.1-10.6 mmol/kg[7]
. Cho is a marker
of brain injury of non-specic type. Cho level reects the
brain membrane metabolism with cellular turnover. The
most prominent peak of Cho in MRS is the resonance
at 3.2 ppm and concentration of 0.9-2.5 mmol/kg[6]
.
Lipids comprise about 20% of brain weight. Lipids are
normally absent from 1H spectrum, and its appearance
at 0.9-1.4 ppm resonances indicates presence of
necrotic tissue (i.e., breakdown of cell membrane and
release of fatty acids)[8]
. The mI is a marker of glial
proliferation. It resonates at 3.6 ppm and concentration
of 3.8-8.1 mmol/kg[9]
. The glutamate/glutamine peak
represents a mixture of excitatory and inhibitory brain
neurotransmitters. Glutamate is mainly stored in
neurons whereas glutamine concentration is higher in
astrocytes. Both, Glx have two groups of resonances,
the first group resonances at 3.6-3.9 ppm whereas
the second group resonances at 2.0-2.6 ppm and
concentration of 6.0-12.5 mmol/kg for glutamate and
3.0-5.8 mmol/kg for glutamine. Excess glutamate in
active lesions could contribute to axonal damage, brain
atrophy and neurological disability[10].Malignant brain tumors are differentiated from
other focal lesions, including multiple sclerosis (MS),
radiation necrosis and infections/abscess by absent
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Hamed SA et al . Vanishing brain lesion: A case presentation
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NAA, excess Cho and lip. Spectra with elevated Cho,
a Cho/Cr index greater than 1.3 and diminished NAA
levels are associated with aggressive neoplasms (e.g.,
malignant lymphoma and glioma). Tumor recurrence
is characterized by high Cho/Cr and Cho/NAA ratios.
A multi-voxel Cho/Cr ratio of > 1.54 and Cho/NAAratio of > 1.05 was found to have 93.1% and
89.7% accuracies for diagnosis of tumor recurrence,
respectively[11,12]
. In MS, the abnormal increases in
total Cr, total Cho, mI, Lac, lipids and macromolecules
are markers for acute demyelination in MS. NAA is
reduced in acute MS lesions and in normal appearing
white matter, even distant to acute and chronic-lesions.
Increased NAA to subnormal values occurs during
remyelination. mI is increased in chronic MS (a marker
for astrocytic gliosis). Reduced NAA peak represents
neuronal/axonal dysfunction or loss. Elevated Cho peak
represents enhanced cell-membrane turnover and is
seen in demyelination, remyelination, inflammation,or gliosis
[13]. In radiation necrosis (dened as a death
of normal brain tissue caused by radiation therapy),
in which the pathological features include progressive
cellular necrosis (coagulative necrosis), inammatory
changes and reactive glial cell proliferation and
gliosis, MRS shows elevated Cho, mI, lactate and lipid
peaks[14]
.
This paper described a child with a symptomatic
parenchymal brain mass but showed marked clinical
recovery and disappearance of the original brain mass
shortly after starting treatment. In this case report, the
phenomenon of a tumor/or pseudo-tumor remissionand the problems related to its differential diagnosis
and treatments were discussed. The significance
of using MRS to distinguish neoplastic from non-
neoplastic nature of the intra-axial lesion in our patient
was also discussed.
CASE REPORT
At September 2009, a 14-year-old child presented with
a history of fever, anorexia, generalized body ache,
loss of weight and headache since two months, which
progressed to repeated vomiting, nausea, lethargy and
blurring of vision in the last month. Prior to neurologic
consultation, the patient was admitted to a fever
hospital for one week because of the unexplained
high grade fever. One year ago, the patient had past
history of body aches and recurrent arthritis which
was attributed to recurrent tonsillitis and based on the
advice of the ear, nose and throat (ENT) physician,
the patient did tonsillectomy. The mother said that
although it was expected that the patient will be
better after tonsillectomy but unfortunately, he had
recurrent fever and generalized body aches till the
time of presentation. On neurological examination,
the child was feverish and looked toxic. He was alert,oriented and his higher mental functions testing were
normal. He had right hemiparesis and right upper
motor neuron facial paralysis. His fundus examination
was normal. MRI-brain [1.5-Tesla, standard (T1W)
pre- and post-contrast, T2W, uid attenuated inversion
recovery (FLAIR) brain imaging] revealed presence
of a large intra-axial mass (25 mm × 19 mm) in the
left temporal lobe with extension to the adjacent
brainstem. It showed hypointense signal in T1W,hyperintense signals in T2W and FLAIR images and
homogenous enhancement with gadolinium (Gd).
It was surrounded by moderate perifocal vasogenic
edema with mass effect in the form of compression
of the third ventricle with midline shift (Figure 1). The
clinical and radiological ndings were highly suggestive
of a neoplastic lesion (malignant lymphoma or glioma).
The patient was examined for lymphadenopathy and
organomegaly. He underwent laboratory workup [for
complete blood count, erythrocyte sedimentation rate
(ESR), glucose, electrolytes, lactic dehydrogenase
(LDH), liver and renal functions], abdominal ultra-
sonography and chest radiographs to rule out thepresence of systemic lymphoma but no bone marrow
evaluation was done. Blood tests revealed leukocytosis
(16000 cells/μL) and elevated ESR (30/52). In view
of the presence of fever, manifestations of increased
intracranial pressure (ICP) and the prominent cerebral
edema associated with the intracranial lesion;
intravenous antibiotics (cefotax 1 g/12 h per 7 d),
mannitol (2 g/12 h per 48 h) and dexamethasone (8
mg/12 h) were initiated. The oncologist recommended
whole craniospinal irradiation (brain = 4000 CGy/20
settings per 4 wk; spine = 2600CGy/13 settings per
3 wk) which was started 10 d after presentation.Within 15 d and even before the start of radiotherapy,
the patient exhibited marked clinical recovery (up to
complete improvement) but he developed subjective
cognitive deterioration as a side effect of radiotherapy
which was recovered after its discontinuation. Tapering
of steroids was done over the next 4 mo. Follow up
of the patient was done every 3 mo. The follow up
MRI after 3 mo from onset showed disappearance of
the original mass but presence of small lesion with
hypointense signal in T1W and hyperintense in T2W
and FLAIR signals in the antero-medial part of the left
temporal lobe but did not show enhancement with
Gd. At further follow up (September 2010) the patient
condition was unremarkable and his MRI had the
same small non-enhanced lesion (Figure 2). At August
2012, the patient developed recurrent generalization
tonic-clonic convulsions. His EEG showed left temporal
focus of epileptic activity. His MRI had the same
small non-enhanced lesion (as that of 2010) with no
restricted diffusion in diffusion weighted images (DWI)
(Figure 3). The seizures frequency was reduced with
carbamazepine therapy (300 mg/12 h). At October
2014, his follow up MRI had the same small non-
enhanced lesion (as that of 2010 and 2012) with no
restricted diffusion in DWI. Single voxel proton (1H)spectroscopy at long and short echo times showed
reduced values of choline to creatine (Cho/Cr: long
ET = 0.05; short ET = 0.907), N-acetyl-aspartate to
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gliotic lesion (Figure 4).This study was conducted according to the prin-
ciples established in Helsinki and approved by Assiut
University Hospital ethics committee. Informed written
creatine (NAA/Cr: long ET = 1.31; short ET = 1.107)and N-acetyl-aspartate to choline (NAA/Cho: long ET
= 0.037; short ET = 0.38) ratios which conrmed the
absence of neoplastic activity but highly suggestive of
Figure 1 Cranial magnetic resonance imaging brain (on admission at September 2009) showing (A, B) sagittal and axial T1-weighted views with a solitary
hypointense lesion in the left temporal lobe; (C-E) axial uid attenuated inversion recovery and T2-weighted (F) images showing hyperintense lesion in
the left temporal lobe encroaching on the adjacent brainstem with perifocal edema and mass effect; (G, H) axial and sagittal T1-weighted views showing
homogenous solitary enhanced lesion in the left temporal lobe encroaching on the adjacent brainstem and surrounded by a moderate hypointensity.
A B C D
E F G H
Figure 2 Cranial magnetic resonance imaging brain (September 2010) showing (A, B) normal axial and sagittal TIW and (C) axial T2W images but (D)
hyperintense lesion in the antero-medial region of the left temporal lobe (white arrow) in uid attenuated inversion recovery image.
Figure 3 Cranial magnetic resonance imaging brain (August 2012) showing (A, B) hyperintense lesion in the antero-medial region of the left temporal lobe
(white arrow) in axial uid attenuated inversion recovery images (white arrow) and (C, D) normal diffusion weighted axial images.
A B C D
A B C D
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consent was obtained from the patient and his parents
to publish the details of his clinical history, laboratory
and imaging data.
DISCUSSION
This case is significant as the parenchymal brain
mass could not be distinguished from a neoplastic
space occupying lesion (e.g., glioma or lymphoma)
at presentation. Brain biopsy was not done due
to deep location of the lesion. Complete clinical
improvement was observed within 15 d on medical
treatment including steroids and even before the
start of radiotherapy. Corticosteroids were used
empirically to reduce the manifestations of increased
ICP and improve the surrounding vasogenic edema
caused by the intracranial mass. The decision to give
whole craniospinal irradiation was based on the high
suspicion of a neoplastic lesion (e.g., lymphoma or
glioma). Marked reduction of the intracranial mass
with disappearance of enhancement was observed in
MRI within 3 mo of the onset. Follow up of the patients
up to 5 years showed absence of recurrence of the
original lesion.
Based on the above findings, the suggestivedifferential diagnosis of the vanishing space occupying
lesion in this child at presentation include: (1) tumor
[e.g., primary central nervous system lymphoma
(PCNSL) or glioma]; (2) tumor like demyelinating
lesion or tumefactive multiple sclerosis (TMS); in
clinical practice, most vanishing brain masses are
frequently diagnosed as malignant tumors or multiple
sclerosis (MS); and (3) intracranial infection/abscess/
granulomas or tuberculoma.
For our patient, earlier at presentation, PCNSL was
suggested. In patients presented with unclear intra-
axial brain masses which regress with steroids, the
diagnosis of PCNSL has to be considered[15]
. PCNSL is
a rare extranodal non-Hodgkin’s lymphoma[16]
. PCNSL
represents approximately 3%-4% of newly diagnosed
A B C
D
E
Figure 4 Cranial magnetic resonance imaging and magnetic resonance spectroscopy (MRS) brain (October 2014) showing (A, B) hyperintense lesion
in the antero-medial region of the left temporal lobe in axial and coronal uid attenuated inversion recovery images (white arrow); and (C) no restricted
diffusion in axial diffusion weighted axial images; (D, E) long and short time echo MRS showing reduced values of Cho/Cr (long ET = 0.05; short ET = 0.907),
NAA/Cr (long ET = 1.31; short ET = 1.107) and NAA/Cho (long ET = 0.037; short ET = 0.38) ratios. NAA: N-acetyl-aspartate; Cr: Creatine; Cho: Choline.
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central nervous system (CNS) tumors[17]
. The typical
MRI features of PCNSL include the presence of intra-
axial single or multiple masses adjacent to cerebrospinal
fluid space (CSF) with intermediate- to low-signal-
intensity in T1W images and hypointense signal rela-
tive to the gray matter on T2W images, surroundingvasogenic edema, mass effect, restricted diffusion
in DWI and intense homogenous enhancement with
Gd[18,19]
. Although, PCNSL is extremely rare in children
and immunocompetent individuals[20,21]
, we suggested
the diagnosis of PCNSL based on the MRI appearance of
large solitary deep hemispheric inltrative lesion
[22] and
rapid remission with steroid even before the start of
radiotherapy. However, PCNSL is a malignant neoplasm
and never considered as a self-limiting and recurrence
is common within 18 mo. No cases have been reported
yet for malignant brain tumors that recurred more
than 5 years after spontaneous regression[23]
. For our
patient, the lacks of recurrence on follow ups for morethan 5 years making such diagnosis less likely. This was
also confirmed by the findings of MRS which will be
discussed in the following section.
Also for our patient, the presence of fever prior to
presentation and rapid remission with Ⅳ antibiotics
and steroid suggest the diagnosis of TMS[24]
or abscess/
granuloma[25]
but not the diagnosis of tuberculoma[26]
.
TMS is defined as a solitary large intracranial lesion
larger than 2.0 cm in diameter associated with peri-
lesional edema and mass effect[24]
. TMS represents
1-2/1000 of cases of MS. TMS has been reported to be
extremely rare in children in comparison to tumors andabscesses
[27]. Diagnosis of MS depends on combination
of clinical, neurophysiological, elevation of CSF im-
munoglobulin G (IgG) index and oligoclonal bands,
and MRI of the brain and spine. Immunosuppressants
(including steroids) and immunomodulators are the
main therapies of TMS[28]
. TMS lesion usually appears
as open-ring (directed toward the cortical surface or
to the basal ganglia) or closed ring or has diffuse,
homogeneous, punctate, or concentric enhance-
ment with Gd[29]
. Although, CSF examination and
gadolinium-enhanced MRI scan should differentiate
between the MS and PCNSL, however, CSF may also
be normal in fulminant conditions and short duration of
the disease[30]
.
Furthermore, for our patient inflammatory pseu-
dotumors or non-neoplastic lesions (e.g., abscess/
granulomas) of unknown etiology and respone to
steroids was also suggested[25]
. Patients with intracranial
infection/abscess/granulomas commonly have history
of risk factors (e.g., immunocompromised state,
dental, pulmonary or ear abscesses and intravenous
drug use), fever, abnormal labs (as high erythrocytic
sedemintation rate or C-reactive protein) and abnormal
CSF suggesting CNS infection. Presentation is usually
of acute onset with manifestations of increased ICP,seizures and focal neurological deficits. MRI-brain of
brain abscess usually shows ring enhancement which is
often complete with regular margin[31]
.
Magnetic resonance spectroscopy (MRS) was
not done to the patient at presentation (2009) to
distinguish neoplastic from non-neoplastic nature
of the mass due to lack of availability. However and
fortunately, it was available later and was done to
the patient when he developed epilepsy (2012).For our patient, the focal lesion in the left antero-
medial region of the temporal lobe found in the MRI
(2010-2014) is the cause of the patients’ left temporal
lobe epilepsy with secondary generalization. The
suggested differential diagnosis of the lesion according
to the conventional MRI include: (1) tumor recurrence;
(2) radiation necrosis; (3) multiple sclerosis; and (4)
post-infective/inflammatory gliosis. MRS helped to
distinguish tissue changes due to different brain lesions
as discussed below.
For our patient, the reduced Cho/Cr (short ET =
0.907; long ET = 0.05), NAA/Cr (short ET = 1.107;
long ET = 1.31) and NAA/Cho (short ET = 0.38;long ET = 0.037) ratios confirm the absence of
tumor recurrence. Furthermore, the lack of reduced
diffusion in DWI also confirms the absence of tumor
recurrence[32]
.
For our patient, the diagnosis of radiation necrosis
was suggested based on the facts that children are
more susceptible to radiation necrosis than adults[33]
and it usually occurs approximately 2-32 mo after
radiotherapy, with 85% of cases occurring within 2
years. Delayed radiation-induced brain injury is a
relatively common complication of radiation therapy
representing 3%-24%[34]
. Radiation necrosis isusually presented as a solitary periventricular white
matter lesion, because of excess oligodendrocytes in
these areas and a poor blood supply that produces
ischemia[35]
. The typical MR appearance of radiation
necrosis is a soap bubble or Swiss cheese-like
enhancing periventricular mass[36-38]
and elevated
Cho, mI, lactate and lipid peaks in MRS[39,40]
. Radiation
necrosis is related to both the volume of irradiated
brain and the total administered radiation dose[41]
.
It has been reported radiation necrosis is extremely
rare (5%) at doses < 45 Gy given over 25 fractions,
or when the fractional dose is < 2 Gy/d but often
occurs with total doses of > 60-70 Gy[34]
or when the
fractional dose is ≥ 2 Gy/d. Our patient was given
whole brain radiotherapy in a dose of 4000 CGy/20
settings per 4 wk (i.e., < 2 Gy/d) making the diagnosis
of radiation necrosis less likely. Also the absence of
enhancement of the new lesion further conrms that
the lesion in our patient is not a radiation necrosis.
Although, the results of MRS of our patients may
suggest remyelination and gliosis following TMS,
however, the presentation with seizures and lack of
relapse with enhanced lesions after 5 years of follow
up makes the diagnosis of MS less likely[13]
.
For our patient, the reduced values of Cho/Cr,NAA/Cr and NAA/Cho and lack of enhancement of
the lesion are consistent with the diagnosis of gliosis.
Gliosis is the process of scarring in the central nervous
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system[42]
. It results from the proliferation of glial cells
or in a damaged brain tissue. It represents a healing
process of brain injury whatever its nature. When
neurons are injured, astrocytes proliferate in the
region and manufacture glial-fibrillary acidic protein.
This compound causes the astroglia to form a denseand brous tissue: The glial scar. Gliosis can take from
a few days to many months to reach its final form.
Gliosis is diagnosed by immunohistochemistry or
MRI[43]
. Gliosis occurred as a result of an acquired brain
injury (most likely abscess, granuloma, inammation)
and it is the cause of temporal lobe epilepsy. Cr and
Cho are glial markers. Gliosis typically presents with
reduced levels of Cho, NAA, and Cr and observed lip
peaks. Moderate levels of Cho and/or a Cho/Cr index
< 1.3 are frequent with gliosis. This is supported by
the followings: (1) the development of epilepsy in our
patient occurred as a result of a focal lesion in the
antero-medial region of the left temporal lobe whichis suggestive of gliosis with no evidence of neoplastic
activity as conrmed by MRS; and (2) mesial temporal
lobe epilepsy (due to hippocampal sclerosis) is
characterized by hippocampal atrophy, decreased NAA,
and a low NAA/Cr ratio which are attributed to neuron
loss and gliosis[39]
.
ACKNOWLEDGMENTS
I would like to thank the patient’s parents for their
cooperation and providing approval to publish the
clinical, laboratory and imaging results of this casepresentation.
COMMENTS
Case characteristics A 14-year-old child with history of acute manifestations of increased intracranial
pressure and right sided hemiparesis which improved completely within two
weeks and followed after 3 years by epilepsy.
Clinical diagnosisThe patient was having right sided hemiparesis due to brain space occupying
lesion which was complicated by recurrent generalized epilepsy.
Differential diagnosisBrain tumor (e.g., primary central nervous system lymphoma or glioma); tumor
like demyelinating lesion or tumefactive multiple sclerosis and intracranial
infection or abscess/granulomas.
Laboratory diagnosisBlood tests revealed mild leukocytosis and elevated erythrocyte sedimentation
rate (ESR).
Imaging diagnosisInitially at presentation, magnetic resonance imaging-brain showed a large
intra-axial mass (25 mm x 19 mm) in the left temporal lobe with hypointense
signal in T1W, hyperintense signals in T2W and fluid attenuated inversion
recovery (FLAIR) images and homogenous enhancement with Gd suggesting
neoplastic lesion (malignant lymphoma or glioma) while follow up after 5 years,
MRI showed small non-enhanced lesion in the antero-medial part of the left
temporal lobe with hypointense signal in T1W and hyperintense in T2W and
FLAIR signal and reduced choline (Cho)/creatine (Cr), N-acetyl-aspartate (NAA)/
Cr and NAA/Cho ratios in magnetic resonance spectroscopy (MRS) which
conrmed absence of neoplastic activity but suggestive of gliosis.
Pathological diagnosisInammatory brain space occupying lesion complicated by gliotic lesion in the
antero-medial part of the left temporal lobe.
Treatment Brain dehydrating measures, antibiotics, corticosteroids and a course of
craniospinal irradiation.
Related reportsIn clinical practice; a vanishing brain space occupying lesion is commonly
diagnosed as a neoplasm (e.g., lymphoma) or multiple sclerosis.
Term explanation A va nish ing brai n spac e occu py ing le si on is de fine d as reduct ion or
disappearance of a brain lesion spontaneously or after steroid treatment to ≤
70% of its size before establishing its denitive diagnosis.
Experiences and lessonsIn clinical practice, neuroimaging [including MRS or magnetic resonance
imaging (MRI)] has to be done every 6-12 mo for at least 3-5 years to follow up
after complete remission of the patient with a vanishing brain lesion.
Peer-review The case report presents a vanishing brain space occupying lesion in a
child over 5 years course of recovery and MRI follow-up. The prognosis
was fortunately better. Text is well wrote and easily comprehensible with
clear figures. The authors discussed the potential differential diagnosis, and
recommended that MRS may be helpful to identify a potential vanishing brain
space occupying benign lesion from tumor lesion in clinic.
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P- Reviewer: Amiri M, Jiang B S- Editor: Tian YL
L- Editor: A E- Editor: Wang CH
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